MuscleLedger

Creatine vs Peptides: What the Trial Count Shows

One side has 2,788 randomised human trials and a small effect; the other has none and a large promise. Both halves reported, including who funded the research.

MuscleLedger Editorial · Published 2026-09-06

The comparison that sells peptides is against nothing. A vendor page describes what a compound does in rats and lets the reader supply the benchmark. Set an actual benchmark next to it — the cheapest, most-studied ergogenic aid in the building — and the shape of the argument changes, in both directions. Creatine's advantage is enormous in evidence and small in effect. This page reports both halves. It is research journalism about research compounds and contains no usage guidance, per our editorial standards.

The count

Searched on PubMed, 2026-09-06.

Compound Human evidence on PubMed
Creatine 2,788 randomised controlled trials in humans; 457 meta-analyses
BPC-157 0 clinical trials (clinical-trial or RCT publication filter)
Ipamorelin 2 randomised human trials, neither with a muscle endpoint
CJC-1295 33 records of any kind, all species and designs
MK-677 (ibutamoren, not a peptide) 63 records of any kind
AOD-9604 22 records of any kind

The ratio between the first row and the rest is the argument. It is also the reason this site's evidence ledger scores creatine 5 and the injectables 1 or 2 — the rubric rewards replicated human trials, and only one column of this table has any.

Now the uncomfortable half: how big is creatine's effect?

Small. This deserves saying clearly, because the supplement industry overstates it and because a publication that only polices peptide claims is not being consistent.

The largest meta-analysis of the classic literature pooled 100 placebo-controlled studies and calculated effect sizes across 163 body-composition outcomes. The result: 0.17 for body composition, 0.24 for tasks lasting 30 seconds or less, 0.19 for glycolytic work. The paper's own conclusions note that the effect was larger for upper-body than lower-body exercise and that creatine "does not appear to be effective in improving running and swimming performance" (Branch, International Journal of Sport Nutrition and Exercise Metabolism 2003).

The modern estimate, restricted to trials that measured muscle directly with MRI, CT or ultrasound rather than inferring it from body mass, is smaller. Burke and colleagues analysed 44 outcomes across 10 studies of at least six weeks and found a pooled estimate of 0.11, with a 95% credible interval from -0.02 to 0.25 — "a very small effect favoring creatine supplementation when combined with resistance training" — and site-specific gains of 0.10 to 0.16 cm in muscle thickness (Burke et al., Nutrients 2023, PMC10180745).

A tenth of a centimetre of muscle thickness, with a credible interval that touches zero, is not a transformation. It is a real, replicated, cheap and legal edge, and it is the largest such edge anyone in this comparison can document.

Who paid for the creatine literature

Worth stating, because it is the objection a fair reader should raise. The 2023 imaging meta-analysis carries a conflict-of-interest statement disclosing a former scientific advisory board role at a supplement manufacturer that sells creatine, industry-sponsored creatine research, creatine donations and conference travel support, expert-witness and consultancy work in creatine litigation, and sales of creatine educational videos. The 2021 review of creatine in women's health discloses that two of its four authors advise a creatine manufacturer, with the note that the company had no role in the content.

These disclosures are printed in the papers and are easy to check. Two observations follow. The findings they produced are conspicuously unflattering — an effect size of 0.11 with an interval crossing zero is not what a sponsored analysis usually delivers. And the comparison compound has no equivalent disclosure to examine, because it has no trials to disclose interests in. An absent literature cannot have a conflict of interest, and that is not a point in its favour.

What the peptide side would need to show

Not more mechanism. A randomised, placebo-controlled trial in trained adults, with a strength or muscle-size endpoint measured by imaging, powered to detect something. That trial has not been run for BPC-157, TB-500, CJC-1295, ipamorelin, sermorelin or IGF-1 LR3.

The nearest approach is instructive. Ipamorelin's one randomised human trial was in postoperative ileus after bowel resection — a gut-motility question, not a muscle one — and it did not meet its endpoint: median time to a first tolerated meal was 25.3 hours on ipamorelin against 32.6 on placebo, p = 0.15, in 114 analysable patients (Beck et al., International Journal of Colorectal Disease 2014). The class has one properly randomised, placebo-controlled human result and it is null.

Growth hormone itself, the thing all the secretagogues are marketed as a route to, has been tested in healthy adults and the outcome is the ceiling for the whole category: a meta-analysis of 18 study populations and 220 treated participants found fat mass down 2.1 kg and lean body mass up 2.1 kg, with weight unchanged, alongside significantly increased rates of soft-tissue oedema, arthralgia, carpal tunnel syndrome and gynecomastia. Its conclusion was that growth hormone "cannot be recommended" for this use (Liu et al., Annals of Internal Medicine 2007). No strength outcome was synthesised. MuscleLedger's page on muscle-and-fat-loss claims works through what that 2 kg each way does and does not mean.

The part that is not about efficacy at all

For anyone in a tested pool, the comparison ends before the effect sizes. Creatine is not on the WADA Prohibited List. BPC-157 is named at S0, thymosin-beta-4 and its derivatives including TB-500 at S2.3, and the growth-hormone secretagogues at S2.2 — prohibited at all times, in and out of competition, with the NCAA's 2026-27 classes naming the same compounds. Our page on peptides and drug testing covers which tests actually look and which do not; the answer changes nothing about the prohibition.

The supply side differs too. Creatine monohydrate is a commodity food supplement. The research compounds reach buyers through a research-use-only channel that the 2026 Sports Medicine review by Mendias and Awan describes as "a parallel 'gray market' of unapproved compounds… operating largely outside of regulatory oversight", with "rigorous human safety data… scarce" (Mendias and Awan, Sports Medicine 2026). Purity and identity are not verified by anyone in that chain by default.

The honest summary

Creatine's evidence advantage over every research compound in this category is close to total: thousands of randomised human trials against zero. Creatine's effect advantage over doing nothing is small and getting smaller as measurement improves. Both of those are true at once, and a page that reports only the first is selling something.

Sources and dates

Frequently asked questions

Is creatine better than peptides for building muscle?

On the evidence, yes, but the honest version of that sentence is less dramatic than it sounds. Creatine's measured effect on muscle size is small — a pooled effect size of 0.11 in the best-controlled meta-analysis, with a credible interval that crosses zero, and 0.10-0.16 cm of muscle thickness at specific sites. It wins the comparison because the research compounds have no measured effect at all: no randomised human trial of any of them reports a strength or muscle-size endpoint in trained adults.

How many human trials of creatine are there compared with peptides?

On PubMed on 2026-09-06: 2,788 randomised controlled trials of creatine in humans and 457 meta-analyses, against zero clinical trials of BPC-157, two randomised human trials of ipamorelin (neither about muscle), and 33 records of any kind for CJC-1295. The comparison is not close, and it is not close in the direction that the pricing of these products would suggest.

Does creatine actually work, or is that overstated too?

It works, modestly, and the modesty is the point. The 2003 meta-analysis of 100 placebo-controlled studies found an effect size of 0.17 for body composition; the 2023 meta-analysis restricted to direct imaging found 0.11, with a credible interval running from -0.02 to 0.25. That is a small, real, repeatedly measured effect. A publication that inflates it is making the same mistake as one that inflates a peptide claim, with better raw material.

Is creatine research funded by the creatine industry?

Substantially, and the papers say so. The authors of the 2023 imaging meta-analysis disclose a former scientific advisory board role at a supplement manufacturer, industry-sponsored creatine research, creatine donations and travel support, expert-witness work in creatine litigation, and sales of creatine educational videos. That does not invalidate the findings — the effect sizes they report are small, which is not what industry-flattering analysis usually produces — but a reader is entitled to know.

Is creatine allowed in tested sport?

Creatine does not appear on the WADA Prohibited List and is not prohibited in or out of competition. The research compounds this page compares it against are prohibited at all times: BPC-157 at S0, thymosin-beta-4 derivatives including TB-500 at S2.3, and the growth-hormone secretagogues at S2.2. For an athlete in a tested pool, that difference outweighs every efficacy argument on this page.

Why do peptides cost more than a supplement with better evidence?

Price in this market tracks novelty and channel, not evidence. Creatine monohydrate is a commodity made at scale with a forty-year literature; the research compounds are sold through a research-use-only channel that a 2026 Sports Medicine review describes as a gray market operating largely outside regulatory oversight. Nothing in the cost of the vial reflects a trial that was run.